'Virtual biopsy' device to detect skin tumors

Using sound vibrations and pulses of near-infrared light, a Rutgers University scientist has developed a new "virtual biopsy" device that can quickly determine a skin lesion's depth and potential malignancy without using a scalpel.

The ability to analyze a skin tumor non-invasively could make biopsies much less risky and distressing to patients, according to a report in Wiley Online Library. Currently, physicians who perform surgical biopsies often don't know the extent of a lesion and whether it will be necessary to refer the patient to a specialist for extensive tissue removal or plastic surgery until surgery has already begun.

The first-of-its-kind experimental procedure, called vibrational optical coherence tomography (VOCT), creates a 3-D map of the legion's width and depth under the skin with a tiny laser diode. It also uses soundwaves to test the lesion's density and stiffness since cancer cells are stiffer than healthy cells. An inch-long speaker applies audible soundwaves against the skin to measure the skin's vibrations and determine whether the lesion is malignant.

"This procedure can be completed in 15 minutes with no discomfort to the patient, who feels no sensation from the light or the nearly inaudible sound. It's a significant improvement over surgical biopsies, which are invasive, expensive and time consuming," said Frederick Silver, a professor of pathology and laboratory at Rutgers Robert Wood Johnson Medical School.

The study found that a prototype VOCT device, which awaits FDA approval for large-scale testing, is able to accurately distinguish between healthy skin and different types of skin lesions and carcinomas. The researchers tested the device over six months on four skin excisions and on eight volunteers without skin lesions. Further studies are needed to fine-tune the device's ability to identify a lesion's borders and areas of greatest density and stiffness, which would allow physicians to remove tumors with minimally invasive surgery.

An important announcement regarding our upcoming conference 12^th World Congress on Cell & Tissue Science (Cell Tissue Science 2019) scheduled on September 13-14,2019 in Singapore. You can also present your latest research at the different topics such as Cancer Cell Biology, Stem Cell & its applications and many more along with other distinguished professors, doctors and researchers from all over the world.

If interested kindly proceed with submitting your abstract and latest biography along with a photography to our online abstract submission page given below: Link for submission: Click Here

Source: https://www.sciencedaily.com/releases/2019/06/190613103129.htm

AI predicts cancer patients' symptoms

Doctors could get a head start treating cancer thanks to new AI developed at the University of Surrey that is able to predict symptoms and their severity throughout the course of a patient's treatment.

The study was first of its kind published in the PLOS One journal. Researchers from the Centre for Vision, Speech and Signal Processing (CVSSP) at the University of Surrey shared the detail how they created two machine learning models that are both able to accurately predict the severity of three common symptoms faced by cancer patients  are depression, anxiety and sleep disturbance. All three symptoms are associated with severe reduction in cancer patients' quality of life.

Researchers analysed existing data of the symptoms experienced by cancer patients during the course of computed tomography x-ray treatment. The team used different time periods during this data to test whether the machine learning algorithms are able to accurately predict when and if symptoms surfaced.

The results found that the actual reported symptoms were very close to those predicted by the machine learning methods.

This work has been a collaboration between the University of Surrey and the University of California in San Francisco (UCSF). The UCSF research in this joint collaboration is led by Professor Christine Miaskowski.

Payam Barnaghi, Professor of Machine Intelligence at the University of Surrey, said: "These exciting results show that there is an opportunity for machine learning techniques to make a real difference in the lives of people living with cancer. They can help clinicians identify high-risk patients, help and support their symptom experience and pre-emptively plan a way to manage those symptoms and improve quality of life."

Nikos Papachristou, who worked on designing the machine learning algorithms for this project, said: "I am very excited to see how machine learning and AI can be used to create solutions that have a positive impact on the quality of life and well-being of patients."

Researchers from different part of the world are invited to submit abstract on their unpublished latest research at our upcoming conference Cell Tissue Science 2019 which is focused on the complications and consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology,Technical Advancements in cancer treatment and many more. We as committee members of the conference welcome you to be a part of the conference “ 12th World Congress on Cell & Tissue Science” in Singapore on March 11-12, 2019. 

You can submit your abstract on Session or Track : 07. Cancer Cell Biology

With Regards to Christmas and New Year Celebration we are providing a special discount of 30% on all Registration Categories for more information please  visit by Click Here

New blood test developed for early diagnosis of ovarian cancer

Research on a bacterial toxin first discovered in Adelaide has led to the development a new blood test for the early diagnosis of ovarian cancer - a disease which kills over 1000 Australian women and 150,000 globally each year.

The new blood test has the potential to dramatically improve early detection of the disease, although it will require further testing before it is available for clinicians.

A research team from the University of Adelaide and Griffith University have been studying the interactions between the toxin and an abnormal glycan (sugar) expressed on the surface of human cancer cells and released into the blood.

The team has now engineered a harmless portion of the toxin to enhance its specificity for the cancer glycan and used this to detect it in blood samples from women with ovarian cancer.

A paper published this month in Biochemical and Biophysical Research Communications has shown that the new test detected significant levels of the cancer glycan in blood samples from over 90% of women with stage 1 ovarian cancer and in 100% of samples from later stages of the disease, but not in any of the samples from healthy controls.

"Ovarian cancer is notoriously difficult to detect in its early stages, when there are more options for treatment and survival rates are better. Our new test is therefore a potential game changer," says Professor James Paton, Director of the University of Adelaide's Research Centre for Infectious Diseases.

Professor Michael Jennings, Deputy Director of the Institute for Glycomics at Griffith University, said: "Detection of this tumor marker may also play a role in a simple liquid biopsy to monitor disease stage and treatment."

The team is currently seeking scientific and commercial partners to further test the technology with larger numbers of patient samples and to adapt it for mass screening.

We welcome researchers from different part of the to submit abstract on their latest research at our upcoming conference Cell Tissue Science 2019 which is mainly focuses on the complications the consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology , Technical Advancements in cancer treatment and many more.We welcome you to the our upcoming conference “ 12th World Congress on Cell & Tissue Science” . 

You can submit your abstract on Session or Track : 8.Advancement in Cancer Treatment

Nutritional supplement can slow cancer growth and enhance effects of chemotherapy

Mannose sugar, a nutritional supplement, can both slow tumor growth and enhance the effects of chemotherapy in mice with multiple types of cancer.

This lab study is a step towards understanding how mannose could be used to help treat cancer.

The results of the study, which was funded by Cancer Research UK and Worldwide Cancer Research, are published in Nature.

Tumors use more glucose than normal, healthy tissues. However, it is very hard to control the amount of glucose in your body through diet alone. In this study, the researchers found that mannose can interfere with glucose to reduce how much sugar cancer cells can use.

Professor Kevin Ryan, lead author from the Cancer Research UK Beatson Institute, said: "Tumors need a lot of glucose to grow, so limiting the amount they can use should slow cancer progression. The problem is that normal tissues need glucose as well, so we can’t completely remove it from the body. In our study, we found a dosage of mannose that could block enough glucose to slow tumor growth in mice, but not so much that normal tissues were affected. This is early research, but it is hoped that finding this perfect balance means that, in the future, mannose could be given to cancer patients to enhance chemotherapy without damaging their overall health.”

The researchers first examined how mice with pancreatic, lung or skin cancer responded when mannose was added to their drinking water and given as an oral treatment. They found that adding the supplement significantly slowed the growth of tumors and did not cause any obvious side effects.

To test how mannose could also affect cancer treatment, mice were treated with cisplatin and doxorubicin - two of the most widely used chemotherapy drugs. They found that mannose enhanced the effects of chemotherapy, slowing tumor growth, reducing the size of tumors and even increasing the lifespan of some mice.

Several other cancer types, including leukemia, osteosarcoma, ovarian and bowel cancer, were also investigated. Researchers grew cancer cells in the lab and then treated them with mannose to see whether their growth was affected. Some cells responded well to the treatment, while others did not. It was also found that the presence of an enzyme that breaks down mannose in cells was a good indicator of how effective treatment was.

Professor Kevin Ryan added:"Our next step is investigating why treatment only works in some cells, so that we can work out which patients might benefit the most from this approach. We hope to start clinical trials with mannose in people as soon as possible to determine its true potential as a new cancer therapy.”

Mannose is sometimes used for short periods to treat urinary tract infections, but its long-term effects have not been investigated. It’s important that more research is conducted before mannose can be used in cancer patients.

Martin Ledwick, Cancer Research UK’s head nurse, said:"Although these results are very promising for the future of some cancer treatments, this is very early research and has not yet been tested in humans. Patients should not self-prescribe mannose as there is a real risk of negative side effects that haven’t been tested for yet. It’s important to consult with a doctor before drastically changing your diet or taking new supplements.”

We welcome researchers from different part of the to submit abstract on their latest research at our upcoming conference Cell Tissue Science 2019 which is mainly focuses on the complications the consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology , Technical Advancements in cancer treatment and many more.We welcome you to the our upcoming conference “ 12th World Congress on Cell & Tissue Science” . 

You can submit your abstract on Session or Track : 8.Advancement in Cancer Treatment

Secrets of engineered protein receptor, CAR

Cancer remains the second-leading cause of death in the United States. This year, an estimated 1.7 million new cases will be diagnosed, with nearly 610,000 people expected to die from the disease, according to the National Cancer Institute.

Fortunately, several recent cancer treatments show considerable promise. Among them is Chimeric Antigen Receptor (CAR) T cell therapy, which the American Society of Clinical Oncology recently named the "2018 Advance of the Year." Three USC Viterbi School of Engineering researchers, Assistant Professor Stacey Finley, Professor Pin Wang and Assistant Professor Nick Graham have just published a paper in "Biophysical Journal" that sheds light on how this new treatment works, information that could one day result in better cancer therapies with fewer side effects.

"We're trying to dig into the molecular mechanisms," said Graham,Chemical Engineering and Materials Science. "By understanding how the CAR T cells work, we could try to design better ones."

When the immune system functions normally, immune cells move around the body and look for pathogens that don't belong and kill them. However, cancer cells can mask themselves, making it harder for the good cells, such as T cells, to kill them.

With CAR T cell therapy, a person's T cells are removed, genetically engineered with proteins, and then injected back into the patient. The resulting CAR T cells are much better at fighting cancer cells. That's because these modified CAR T cells have an engineered protein receptor, the CAR, that can bind to cancer cells. When this occurs, a signal from the CAR tells the T cell to begin destroying the cancer by secreting the chemicals perforin and granzyme.

CAR T cell therapies

Earlier this year, the U.S. Food and Drug Administration approved the first CAR T cell therapy for the treatment of some people with advanced leukemia and a form of lymphoma, both blood cancers. Early results have shown great promise. However, in early tests, the CAR-T cell therapies have so far proven much less effective against breast, lung, prostate and other solid-tumor cancers. Additionally, some people undergoing CAR T cell therapy have experienced significant side effects; a few have even died.

The trio of USC researchers hope their work will greatly improve CAR T cell therapies by uncovering the complicated process by which CARs activate cancer fighting cells. Specifically, they are examining a process called phosphorylation, which is a chemical reaction that occurs when the CAR receptor bumps up against a cancer cell and sends a signal to the T cell to attack the bad cells.

"I think what's most exciting is that we're really adding to the field an understanding of which sites on the CAR are becoming phosphorylated, how quickly that happens and the amount of phosphorylation of each site," said Finley, the Gordon S. Marshall Early Career Chair.

Through their research, Finley, Wang and Graham have learned when and how much phosphorylation occurs on the CAR's six sites, which, in an imperfect analogy, could be imagined as "docking hubs," in Graham's words.

Additionally, they have found that no "gatekeeper" exists, meaning that no single CAR site must be phosphorylated before the others. Until now, scholars only had a general idea about the phosphorylation process, making it difficult to bioengineer CAR T cells that could successfully fight against complex and complicated breast, lung and other solid-tumor cancers.

Better cancer-fighting CARs

Going forward, Finley, Wang and Graham hope to leverage their findings into engineering more effective cancer-fighting CARs with fewer side effects. This could mean having phosphorylation take place quicker and more intensely at certain CAR sites, depending on the complexity of the targeted cancer cells. Alternately, the USC researchers might engineer CARs to phosphorylate less, thereby preventing the cancer-fighting T- and other cells from becoming too aggressive and killing healthy cells -- a problem that has cropped up with early CAR T cell cancer treatments.

Already, Finley has built quantitative models that holds great promise.

"Once we have these tools and quantitative models, we should be able to apply them to a variety of different designs of CARs," said Finley."Maybe you could use a model, before you do an experiment, to see if this new design would work. Instead of having to do as many tedious experiments in the lab, you could build a predictive mathematical model to screen the best design."

Added Wang, the Zohrab A. Kaprielian Fellow in Engineering and professor of chemical engineering and materials science, and biomedical engineering: "If you want to make the T cells more potent, the question is how best to design the CAR. That's our research's goal, I think."

We welcome researchers from different part of the to submit abstract on their latest research at our upcoming conference Cell Tissue Science 2019 which is mainly focuses on the complications the consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology , Technical Advancements in cancer treatment and many more.We welcome you to the our upcoming conference “ 12th World Congress on Cell & Tissue Science” . 

For more info visit :Cell Tissue Science 2019

Better chemo drug adsorption onto targeted delivery capsules

The efficacy of chemotherapy treatment depends on how effectively it reaches cancerous cells. Increasing targeted delivery could mean decreasing side effects. Scientists are enhancing methods of selectively transmitting active chemotherapy agents and reducing their toxicity by encapsulating chemo drugs into active carbon used as the targeted delivery device.

In a new study, Gabriel Román, National University of the South,Argentina, and colleagues have demonstrated that adding minute amounts of aluminium atoms onto activated carbon atoms helps increase the adsorption onto the delivery carbon capsule of a standard chemotherapy drug, called 5-Fluorouracil (5-FU). This drug is typically used for stomach, colorectal, neck and head cancer treatments. This model could lead to more effective and convenient cancer treatments with fewer side effects by encapsulating the chemo drug into the active carbon, so that it can be taken orally.

In this study its examined that the adsorption of 5-FU on test surfaces made up of activated carbon alone and a version containing a minute dispersion of aluminium within the activated carbon structure. They relied on molecular modelling simulation to predict and display adsorption configuration and energy changes in the two scenarios.

They also found that aluminium inclusion increases the adsorption capacity of active carbon. This is because the addition of the metal increases the interactions of the drug with the atoms of the encapsulation material in areas where it is polarised. The electric charges present in some areas of the surface of the drug interact with the charges of the aluminium atoms on the surface of the capsule material. This means they contribute to improving its adsorption properties as less energy is required for the adsorption and the drug is at a shorter distance from the encapsulation material.

We encourage researchers all around the globe to submit abstract on their latest research at our upcoming conference Cell Tissue Science 2019 which is mainly focuses on the complications the consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology , Technical Advancements in cancer treatment   and many more.We welcome you to the our upcoming conference “ 12th World Congress on Cell & Tissue Science” . For more info visit :Cell Tissue Science 2019

New method promises fewer side effects from cancer drugs

Researchers from Faculty of Science - University of Copenhagen have suggested that Protein research is one of the hottest areas in medical research because proteins make it possible to develop far more effective pharmaceuticals for the treatment of diabetes, cancer and other illnesses.

Proteins have incredibly complex chemical structures that make them difficult to modify. As a result, researchers have been looking for a tool to modify them more precisely, without increasing a drug's side-effects.

"We often run the risk of not being approved by health authorities because protein-based drugs lack precision and may have side-effects. Among other things, this is because of the serious limitations with the tools that have been used up until now," according to Professor Knud J. Jensen, University of Copenhagen's Department of Chemistry.

Together with his research colleague, Sanne Schoffelen, he has developed a new protein-modifying method that promises fewer side-effects and could be pivotal in furthering the development of protein-based pharmaceuticals.

Protein structure is like an intricate ball of yarn

Researchers call the method "His-tag acylation." Among other things, it makes it possible to add a toxic molecule to proteins that can attack sick cells in a cancer-stricken body without attacking healthy ones.

"Proteins are like a ball of yarn, a long thread of amino acids, which are turned up. This method allows us to precisely target these intricate structures, as opposed to making uncertain modifications when we don't know what is being hit within the ball of yarn. In short, it will help produce drugs where we can be far more confident about where modifications are being made, so that side effects can be minimized in the future," says Knud J. Jensen.

Modified proteins must target precisely

The fact that His-tag acylation can accurately target these complex yarn-like protein structures also makes it possible to produce drugs with entirely new characteristics.

For example, researchers can now attach a fluorescent molecule to proteins in such a way that a microscope can be used to track a protein's path through cells. The primary function of these proteins is to transport cancer fighting molecules around to sick cells, so it is important to carefully follow their path throughout the body in order to safely produce medications that don't have unintended side-effects.

 

We welcome researchers all around the globe to submit abstract on their latest research at our upcoming conference Cell Tissue Science 2019 which is mainly focuses on the complications the consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology , Technical Advancements in cancer treatment and many more.We welcome you to the our upcoming conference “ 12th World Congress on Cell & Tissue Science” . For more info visit :Cell Tissue Science 2019

Scientists identify 'Achilles heel' of anaplastic large-cell lymphomas

Latest research from the International ERIA Consortium, led by scientists in Vienna have shown that the same signaling pathway is essential to the growth of cancer cells in various forms of ALCL(Anaplastic large-cell lymphomas are rare cancers of the white blood cells.): TYK2 (tyrosine kinase 2, an important component of the immune system) prevents apoptotic cell death by increasing the production of Mcl1, a special type of protein belonging to the BCL2 family. Due to its unique enzymatic composition, TYK2 is therefore an interesting therapeutic target, making TYK2-specific inhibitors highly promising as new therapeutic agents in ALCL.

A particularly fruitful area of personalized medicine in cancer treatment, where improved diagnostic methods are able to break down cancers into increasingly smaller subcategories, thereby making it possible to apply individual treatment strategies. The molecular analysis of human tumour samples has become a main focus of cancer research.So that we can identify new therapeutic targets and validate them in tumor models which will allows us to improve the clinical management of cancer patients.

However, this faces clinicians with several challenges, including increasingly comprehensive diagnostics as well as the problem of adequately validating this data for smaller patient groups. This is all the more urgent in the case of rare cancers such as ALCL, where the number of patients is so small.

"We were therefore able to regard the TYK2 signals as the Achilles heel of ALCL, since both types of ALCL that we investigated relied on its activity to maintain the essential signal to protect against cell death.Attenuating the TYK2 signal in the cell culture resulted in rapid cell death and, in ALCL model mice, in which TYK2 was genetically switched off, the researchers observed that the laboratory animals survived for longer." explains Olaf Merkel

 

Lukas Kenner, MedUni Vienna and the Ludwig Boltzmann Institute for Cancer Research and co-founder of the European Research Initiative stresses that "We look forward to TYK2 inhibitors, which are currently being developed for treating immunological diseases, being available, since we urgently need better treatments for rare lymphomas"

 

Our conference Cell Tissue Science 2019, mainly focuses on the complications the consequences of Stem Cell, Regenerative Medicine, Cellular Therapy, Cancer Cell Biology , Technical Advancements in cancer treatment   and many more. The speakers from different part of the world will be present their immense research talk on this specific topics. We welcome you to the our upcoming conference “ 12th World Congress on Cell & Tissue Science” .You can also present your latest research at our conference.For more info visit : Cell Tissue Science 2019

Children's bone cancers could remain hidden for years before diagnosis

Scientists from Wellcome Trust Sanger Institute have discovered that some childhood bone cancers start growing years before they are currently diagnosed. Researchers at the Wellcome Sanger Institute and Hospital for Sick Children (SickKids), Canada discovered large-scale genetic rearrangements in Ewing Sarcomas and other children's cancers, and showed these can take years to form in bone or soft tissue. This study will help unravel the causes of childhood cancers and raises the possibility of finding ways to diagnose and treat these cancers earlier in the future.

The research also showed that cancers with the complex genetic rearrangements were more aggressive and could benefit from more intense treatment than other cancers.

Ewing sarcoma is a rare cancer found mainly in bone or soft tissue of young teenagers as they grow, and is the second most commonly diagnosed bone cancer in children and young people. Treatment involves chemotherapy, surgery to remove the affected part of the bone if possible and radiotherapy.

Cancer is a genetic disease and in Ewing sarcoma, two specific genes, EWSR1 and ETS, are fused together. To understand the genetic events leading to this, researchers sequenced and analysed the genomes of 124 tumours. They discovered that in nearly half of the cases, the main gene fusion occurred when the DNA completely rearranged itself, forming complex loops of DNA.

"Many childhood sarcomas are driven by gene fusions, however until now we have not known how or when these key events occur, or whether these processes change at relapse. We found dramatic early chromosomal shattering in 42 per cent of Ewing sarcomas, not only fusing two critical genes together, but also disrupting a number of important areas." says Dr.Adam Shlien, Associate Director of Translational Genetics and Scientist in Genetics & Genome Biology, and co-Director of the SickKids Cancer Sequencing (KiCS)

Surprisingly, the researchers found that the complex DNA rearrangements that cause Ewing sarcoma had occurred years before the tumour was diagnosed. This offers possibilities of finding ways to screen for these cancers to treat them earlier.

Dr Sam Behjati from Wellcome Sanger Institute and University of Cambridge Department of Pediatrics, said: "In principle this study provides evidence that Ewing sarcoma could be detectable earlier, possibly even before it reveals itself as disease. If we could detect these childhood cancers sooner, when tumours are smaller, they would be much easier to treat. Further research is needed, but this possibility of finding a way to diagnose Ewing sarcomas earlier could help patients in the future."

The researchers discovered that Ewing Sarcomas with these complex genetic rearrangements were more aggressive than those with simple gene-fusions, and that any relapses needed different treatments. Understanding this could help clinicians offer the best treatment options for each patient.

Dr. David Malkin,Scientist and co-Director of the SickKids Cancer Sequencing (KiCS) program, said: "As an increasing and diverse number of tumour genome sequences become available, we may be able to define further rearrangement processes that underlie fusion genes and thus unravel the causes of fusion-driven human cancers. Our goal is to better understand these cancers in an attempt to improve treatment and outcomes."

 

Our conference Cell Tissue Science 2019, mainly focuses on the complications the consequences of  Cancer Cell Biology and Technical Advancements in cancer treatment. The speakers from different part of the world will be present their immense research talk on this specific topics. We welcome you to the our upcoming conference “ 12th World Congress on Cell & Tissue Science” .You can also present your latest research at our conference.For more info visit : Celltissue Science 2019

Engineered cancer cells can fight primary and metastatic cancer

What if cancer cells could be re-engineered to turn against their own kind?

A new study led by researchers from Brigham and Women's Hospital : The power of gene editing to take a critical step toward using cancer cells to kill cancer. The reports were promising results in preclinical models across multiple types of cancer cells, establishing a potential roadmap toward clinical translation for treating primary, recurrent and metastatic cancer.

"This is just the tip of the iceberg. Cell-based therapies hold tremendous promise for delivering therapeutic agents to tumors and may provide treatment options where standard therapy has failed. With our technique, we show it is possible to reverse-engineer a patient's own cancer cells and use them to treat cancer. We think this has many implications and could be applicable across all cancer cell types."        says  Dr.Khalid Shah,Director of the Center for Stem Cell Therapeutics and Imaging (CSTI) , BWH Department of Neurosurgery and Faculty at Harvard Medical School and Harvard Stem Cell Institute (HSCI).

The new approach capitalizes on cancer cells' self-homing ability that process in which cancer cells can track the cells of their kind that have spread within the same organ or to other parts of the body. Harnessing this power could overcome drug delivery challenges, helping get therapeutics to tumor sites that may otherwise be difficult to reach.

The team developed and tested two techniques to harness the power of cancer cells. The "off the shelf" technique used pre-engineered tumor cells that would need to be matched to a patient's HLA phenotype and the second technique "autologous" which uses CRISPR technology to edit the genome of a patient's cancer cells and insert therapeutic molecules. These cells could then be transferred back into the patient.

To test both approaches, they used mouse models of primary and recurrent brain cancer and breast cancer that has spread to the brain. They saw a direct migration of engineered cells to the sites of tumors and found evidence that the engineered cells specifically targeted and killed recurrent and metastatic cancer in the mice which in turn treatment increased the survival of the mice. Engineered cells were equipped with a "kill switch" that could be activated after treatment -- PET imaging showed that this kill switch worked to eliminate the cells.

"Our study demonstrates the therapeutic potential of using engineered tumor cells and their self-homing properties for developing receptor-targeted therapeutics for various cancers," said Shah.

Our conference Cell Tissue Science 2019, mainly focuses on the complications the consequences of  Cancer Cell Biology and Technical Advancements in cancer treatment. The speakers from different part of the world will be present their immense research talk on this specific topics. We welcome you to the our upcoming conference “ 12th World Congress on Cell & Tissue Science” .You can also present your latest research at our conference.For more info visit : Celltissue Science 2019

Discovery unlocks secrets behind cancer drug resistance

University of Otago research provides insights into an underlying mechanism that could explain why new cancer therapies to help treat metastatic melanoma do not always work on patients, paving the way for predicting which patients will benefit from certain drugs.

Their findings shed much needed light on why new immune checkpoint inhibitor therapies such as nivolumab and pembrolizumab which is approved by the New Zealand Government for the first time in 2016 to treat metastatic melanoma.

The new immunotherapeutic drugs herald a significant advancement in a cure for cancer. But while they can be effective for some melanoma patients, for others the therapies do not work at all, and most eventually become resistant to immunotherapy treatments.One of the key components of the immune checkpoint mechanism is a protein on the surface of cancer cells called PD-L1 which can potentially be receptive to or block immunotherapy.

The Otago researchers were able to show that an epigenetic modification -- DNA modifications that do not directly alter the DNA sequence, but instead change the frequency by which a cell uses specific genes -- specifically DNA methylation, influences whether PD-L1 is expressed on the cancer cell surface.

Dr Aniruddha Chatterjee, Senior Research Fellow, Department of Pathology,who has already gained national recognition as one of the country's top emerging scientists, jointly led the work published today in a leading international journal from the Cell Press, iScience, together with colleagues Professor Mike Eccles from the Department of Pathology and Professor Peter Hersey from the University of Sydney.

"Currently, there are no reliable biomarkers for predicting benefit from immune therapy in melanoma and these are desperately needed in the clinic,Biomarkers would help choose which patients are likely to benefit and who are not. Many groups worldwide are searching for immune-therapy biomarkers and this Otago discovery of an epigenetic marker appears very promising." Dr Chris Jackson, Researcher from University of Otago's Centre says.

Dr Aniruddha Chatterjee says "The findings suggest epigenetic therapies could be used in clinical trials in combination with immunotherapy in melanoma to treat patients. However, further trials would be needed before this could become a possibility."

The Health Research Council has just this month awarded $1,198,714 to the researchers to continue their work on patients in New Zealand over the next three years. Professor Eccles says "they plan to develop a DNA methylation marker panel that predicts the likelihood of melanoma patients responding to immunotherapy treatment.This work will contribute to selecting the best treatment option for patients, and also for developing new targets for epigenetic therapies."

There is currently no robust biomarker able to predict patient response and also relatively little understanding of the basis for resistance to immunotherapy treatment of melanoma. There is a global effort to unlock the secrets behind resistance to immunotherapy and the Otago researchers believe they may have uncovered a key piece of the puzzle.

DNA methylation is an epigenetic mechanism that plays a key role in switching genes "on" or "off" and helps to determine cellular function. Generally, DNA methylation silences gene expression and has been implicated in cancer.

"Our research provides evidence that it is the global loss of DNA methylation that regulates constitutive expression of the immune checkpoint PD-L1 in melanoma," Dr Chatterjee explains.

The findings have been heralded by the researchers' peers internationally as "highly novel" and a major advance in understanding melanoma biology. Department of Pathology Research Fellow Dr Euan Rodger and PhD student Antonio Ahn also carried out a significant amount of the research work.

Our conference Cell Tissue Science 2019, mainly focuses on the complications the consequences of Cancer Cell Biology and Technical Advancements in cancer treatment. The speakers from different part of the world will be present their immense research talk on this specific topics. We welcome you to the our conference “ 12th World Congress on Cell & Tissue Science” .You can also present your latest research at our conference.For more info: Celltissue Science 2019

Off/on switch for DNA repair protein

Damage to DNA is a daily occurrence but one that human cells have evolved to manage. Mayo researchers have determined how one DNA repair protein gets to the site of DNA damage. The authors say they hope this discovery research will help identify new therapies for ovarian cancer.

While the human genome is constantly damaged, cells have proteins that detect and repair the damage. One of those proteins is called 53BP1. It is involved in the repair of DNA when both strands break. In the publication, Georges Mer, a Mayo Clinic structural biologist, and his team report on how 53BP1 relocates to chromosomes to do its job.

Dr. Mer explains that, in the absence of DNA damage, 53BP1 is inactive and blocked by a protein called "TIRR." Using a visualization technique called X-ray crystallography, the researches showed that TIRR obstructs an area on 53BP1 that 53BP1 uses to bind chromosomes. But what shifts TIRR away from 53BP1, so the repair protein can work?

They theorized that the type of nucleic acid called RNA was responsible for this shift. To test their theory, they engineered a protein that would bind to the 53BP1 repair protein and the RNA molecules released when DNA is damaged. They reported that when DNA damage occurs, RNA molecules produced at that time can bind to TIRR, displacing it from 53BP1 and allowing 53BP1 to swing into action.

"Our study provides a proof-of-principle mechanism for how RNA molecules can trigger the localization of 53BP1 to DNA damage sites. The TIRR/RNA pair can be seen as an off/on switch that blocks or triggers 53BP1 relocation to DNA damage sites. " says Dr. Georges Mer. 

However they reported that displacing TIRR increases sensitivity of cells in cell culture to olaparib, a drug used to treat patients with ovarian cancer.

"Unfortunately, over time cancer cells develop resistance to drugs in this category, called 'PARP inhibitors.Our work provides a new target, TIRR, for developing therapeutics that would help specifically kill ovarian cancer cells," Dr. Mer says.

Our conference Cell Tissue Science 2019, mainly focuses on the complications the consequences of Cancer Cell Biology and Technical Advancements in cancer treatment. The speakers from different part of the world will be present their immense research talk on this specific topics. We welcome you to the our conference “ 12th World Congress on Cell & Tissue Science” .You can also present your latest research at our conference.For more info: Celltissue Science 2019

Fluorescent molecules reveal how cancer cells are inhibited

Researchers from Lund University, Sweden has developed a fluorescent variant of a molecule that inhibits cancer stem cells, which has enabled the researchers to  Capturing images of when the molecule enters a cell using cell-biological methods to successfully describe how and where the molecule counteracts the cancer stem cells.

However, Salinomycin is a molecule produced by terrestrial bacteria of the species Streptomyces albus. It was previously known that this molecule acts selectively against cancer stem cells, but the mechanism behind it was not understood. Anyhow, now the Lund researchers have created a fluorescent variant of salinomycin to understand how it works.

"We have shown where the molecule ends up when it is absorbed by cancer cells. By making the molecule fluorescent, we have also been able to capture the course of events on film" says Dr.Daniel Strand who leads an organic chemistry research team at Lund University.

It has long been known that this molecule can transport ions across cell membranes, in this case potassium ions. Even so, the researchers were surprised when they saw images of the molecule in cells.

Dr.Daniel Strand said, "Those of us involved in the study initially naïvely assumed that the molecule acted in the cell's outer membrane".

However, the images showed that the molecule rapidly passed through the outer cell membrane and its destination was an organelle called the endoplasmic reticulum. This is where the molecule acts as an ion transporter, and it is this specific activity that the researchers have succeeded in connecting to a reduction in the percentage of cancer stem cells.

The research results may contribute new approaches to the development of cancer drugs both for treatment of cancer and for reducing the risk of relapse

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Scientists reveal structure of amino acid transporter involved in cancer

Researchers from the University of Groningen have used cryo-electron microscopy to elucidate the structure of the protein, which may generate leads for drug development. The team relieved that the human glutamine transporter ASCT2 is upregulated in several forms of cancer and also the docking platform for a broad range of pathogenic retroviruses.

In human cells, the ASCT2 protein imports the amino acid glutamine which maintains the amino acid balance in many tissues. The increased amount of ASCT2 in many types of cancer, probably due to the increased demand for glutamine. Moreover, several types of retrovirus infect human cells by first docking on this protein.

ASCT2 is part of a larger family of similar transporters. University of Groningen scientists have resolved the 3D structure of the protein, to understand how this family of amino acid transporters works in turn to help in designing the drugs that block glutamine transport by ASCT2.The human gene for ASCT2 was expressed in yeast cells, and the human protein was purified for imaging.

"The structure was determined at a resolution of 3.85 Å, which revealed striking new insights. It was a challenging target, as it is rather small for cryo-EM. But it also has a nice symmetric trimeric structure, which helps". Credits:  Dr. Cristina Paulino, Assistant Professor of Structural Biology and Head of the University's Cryo-EM Unit

The images from cryo-EM revealed a familiar type of 'lift-structure', in which part of the protein travels up and down through the cell membrane. In the upper position, substrate enters the lift, which then moves down to release the substrate inside the cell. The structure of ASCT2 revealed the lift in the lower position. "To our surprise, this part of the protein was further down then we had ever seen before in similar protein structures", says Dr. Dirk Slotboom, Professor of Biochemistry. "And it was rotated. It had been thought that the substrate enters and leaves the lift through different openings, but our results suggest it might well use the same opening".

"This information could help design molecules that stop glutamine transport by ASCT2. Blocking glutamine transport would be a way to kill cancer cells. This new structure should allow for a more rational design of transport inhibitors", says Dr.Albert Guskov, Assistant Professor in Crystallography

Another surprising observation was the spikes that protrude on the outside of each of the three monomers which they have never been seen before. By knowing the shape of the spikes that could help them to design molecules which will block the viruses from docking.

The protein structure was resolved in about four months, which is remarkably fast for Cryo-EM. Different scientists, each with their own specialty, worked in parallel, which speeded up the process. Furthermore, PhD student Alisa Garaeva, who played a central role in ensuring the project ran efficiently.

“Submit your abstracts for Session 8: Advancement in Cancer Treatment at the following link:  Click Here"